Another study demonstrated that in an endometrial adenocarcinoma cell line, the protein cellular apoptosis susceptibility protein (CAS) stabilizes a complex between E-cadherin and β-catenin, and overexpressed EMMPRIN disrupted this complex, promoting E-cadherin degradation and release of β-catenin, leading to increased EMT [63]. The gene discussed is CSE1L; the disease is endometrium adenocarcinoma.